首页> 外文期刊>European journal of medical research. >Simian Virus 40 Inhibits Differentiation and Maturation of Rhesus Macaque DC-SIGN superset+-Dendritic Cells.
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Simian Virus 40 Inhibits Differentiation and Maturation of Rhesus Macaque DC-SIGN superset+-Dendritic Cells.

机译:猿猴病毒40抑制猕猴DC-SIGN超集+树突细胞的分化和成熟。

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摘要

Dendritic cells (DC) are the initiators and modulators of the immune responses. Some species of pathogenic microorganisms have developed immune evasion strategies by controlling antigen presentation function of DC. Simian virus 40 (SV40) is a DNA tumor virus of rhesus monkey origin. It can induce cell transformation and tumorigenesis in many vertebrate species, but often causes no visible effects and persists as a latent infection in rhesus monkeys under natural conditions. To investigate the interaction between SV40 and rhesus monkey DC, rhesus monkey peripheral blood monocyte-derived DC were induced using recombinant human Interleukin-4 (rhIL-4) and infective SV40, the phenotype and function of DC-specific intracellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) superset+ DC were analyzed by flow cytometry (FCM) and mixed lymphocyte reaction (MLR). Results showed that SV40 can down-regulate the expression of CD83 and CD86 on DC and impair DC-induced activation of T cell proliferation. These findings suggest that SV40 might also cause immune suppression by influencing differentiation and maturation of DC.
机译:树突状细胞(DC)是免疫应答的起始剂和调节剂。某些病原微生物物种通过控制DC的抗原呈递功能而开发了免疫逃逸策略。猿猴病毒40(SV40)是恒河猴起源的DNA肿瘤病毒。它可以在许多脊椎动物中诱导细胞转化和肿瘤发生,但在自然条件下,通常不会引起可见的影响,并作为潜伏感染持续存在于恒河猴中。为了研究SV40与恒河猴DC之间的相互作用,使用重组人白细胞介素-4(rhIL-4)和感染性SV40诱导恒河猴外周血单核细胞衍生的DC,DC特异性细胞内粘附分子3的表型和功能通过流式细胞仪(FCM)和混合淋巴细胞反应(MLR)分析非整联蛋白(DC-SIGN)超集+ DC。结果表明,SV40可以下调DC上CD83和CD86的表达,并削弱DC诱导的T细胞增殖活化。这些发现表明,SV40也可能通过影响DC的分化和成熟而引起免疫抑制。

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